| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2013-08-27 |
| タイトル |
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タイトル |
Protein Kinase A Catalytic Subunit Alters Cardiac Mitochondrial Redox State and Membrane Potential Via the Formation of Reactive Oxygen Species |
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言語 |
en |
| 言語 |
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言語 |
eng |
| キーワード |
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主題 |
Inner membrane anion channel |
| キーワード |
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主題 |
Mitochondrial membrane potential |
| キーワード |
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|
主題 |
Mitochondrial respiratory chain |
| キーワード |
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主題 |
Protein kinase A |
| キーワード |
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主題 |
Reactive oxygen species |
| 資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
| その他のタイトル |
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その他のタイトル |
蛋白質リン酸化酵素AのCatalytic Subunitは活性酸素種形成を介して心臓ミトコンドリアRedox状態と膜電位を変化させる |
| 著者 |
Nagasaka, Shiro
Katoh, Hideki
Niu, Chunfeng
Matsui, Saori
Urushida, Tsuyoshi
Satoh, Hiroshi
Watanabe, Yasuhide
Hayashi, Hideharu
|
| 書誌情報 |
en : Circulation Journal
巻 71,
号 3,
p. 429-436,
発行日 2007-02-20
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| 出版者 |
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出版者 |
THE JAPANESE CIRCULATION SOCIETY |
|
言語 |
en |
| 権利 |
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|
権利情報 |
Copyright 2007 THE JAPANESE CIRCULATION SOCIETY |
| 権利 |
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|
権利情報 |
本文データは学協会の許諾に基づきCiNiiから複製したものである |
| 抄録 |
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内容記述タイプ |
Abstract |
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内容記述 |
Background The identification of protein kinase A (PKA) anchoring proteins on mitochondria implies a direct effect of PKA on mitochondrial function. However, little is known about the relationship between PKA and mitochondrial metabolism. Methods and Results The effects of PKA on the mitochondrial redox state (flavin adenine dinucleotide (FAD)), mitochondrial membrane potential (ΔΨm) and reactive oxygen species (ROS) production were investigated in saponin-permeabilized rat cardiomyocytes. The PKA catalytic subunit (PKAcat; 50 unit/ml) increased FAD intensities by 56.6±7.9% (p<0.01), 2’7’-dichlorofluorescin diacetate (DCF) intensities by 10.5±3.3 fold (p<0.01) and depolarized ΔΨm to 48.1±9.5% of the control (p<0.01). Trolox (a ROS scavenger; 100μmol/L) inhibited PKAcat-induced ΔΨm, FAD and DCF alteration. PKAcat-induced ΔΨm depolarization was inhibited by an inhibitor of the inner membrane anion channel (IMAC), 4,4’-diisothiocyanatostilbene-2,2’-disulfonic acid (DIDS: 1μmol/L) but not by an inhibitor of mitochondrial permeability transition pore (mPTP), cyclosporine A (100 nmol/L). Conclusions PKAcat alters FAD and ΔΨm via mitochodrial ROS generation, and PKAcat-induced ΔΨm depolarization was not caused by mPTP but rather by DIDS-sensitive mechanisms, which could be caused by opening of the IMAC. The effects of PKA on mitochondrial function could be related to myocardial function under the condition of extensiveβ-adrenergic stimulation. |
| ISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
13469843 |
| EISSN |
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収録物識別子タイプ |
ISSN |
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収録物識別子 |
13474820 |
| NII論文ID |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
NAID |
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関連識別子 |
110006224216 |
| 出版社DOI |
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関連タイプ |
isIdenticalTo |
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識別子タイプ |
DOI |
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関連識別子 |
10.1253/circj.71.429 |
| 著者版フラグ |
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出版タイプ |
VoR |
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出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
CircJ-71-429.pdf (581.7 kB)
